Overactive Bladder (OAB) is a urological condition that affects approximately 50 million patients worldwide. A patient suffering from OAB typically experiences sudden yet frequent and unstoppable urges to urinate, even though the bladder may contain only a small amount of urine. This condition is usually associated with frequent and spontaneous contractions of the detrusor muscle, which is located in the bladder wall and surrounds the bladder.
The etiology of OAB is unclear, and indeed there may be multiple possible causes. OAB, however, is most often associated with detrusor muscle overactivity (i.e., frequent and spontaneous contractions of the detrusor muscle). These frequent contractions may fuse into a global and sustained contraction resulting in an urge to urinate. A malfunctioning detrusor muscle may cause overactive bladder. Indeed, there is a body of evidence suggesting that, in comparison with healthy bladders, overactive bladders exhibit localized changes in detrusor muscle morphology. These changes likely originate from defects on cellular and multi-cellular levels and changes in the nervous system. Such nervous system changes have been correlated to the observed local pathological changes in the muscle (e.g., patchy denervation, increased amount of connective tissue between muscle bundles) which may contribute to the abnormal function of the detrusor muscle.
Identifiable underlying causes include the following: nerve damage caused by abdominal or pelvic trauma or surgery, bladder stones, drug side effects, and neurological disease (e.g., multiple sclerosis, Parkinson's disease, stroke, and spinal cord lesions).
Recent evidence suggests that the detrusor muscle may be triggered by chemicals released from the bladder wall when the wall experiences stimulation, including, but not limited to, stretching of the bladder wall or the presence of potassium or a composite/fluid having a specific pH level, all of which may be associated with increasing accumulation of urine. The released chemicals may include adenosine triphosphate, prostaglandins, nitric oxide, and acetylcholine. The release of these chemicals has been linked to over expression of multiple receptors (muscarinic and cholinergic receptors, TRPV, etc.).
Current therapies for OAB include a variety of approaches. Non-invasive procedures include first-line behavioral and medical therapies employing a class of systemic drugs called anticholinergics. For patients who do not react well to drugs, invasive procedures such as neural stimulation or surgery can be more effective. Both invasive and non-invasive treatments target overall bladder function and do not address local or anatomical abnormalities. Recent studies, however, suggest that abnormal activity may originate from one or more distinct anatomical areas of the bladder such as the dome, internal sphincter, or trigone. Therefore, there exists a need for medical devices and methods of treatment capable of identifying and providing therapy to specific areas of the bladder.